Abstracts 1315 to 1481, LB6–LB15

over eighteen years [1].The exact cause of Type 1 Diabetes Mellitus (T1DM) is not known, nor is it preventable with current knowledge, but it can be treated with daily administration of insulin.Patients with this heterogeneous, multi factorial and polygenic disease are at increased risk of diabetic complications due to impaired blood flow with micro vascular complications, such as, retinopathy, neuropathy and nephropathy, and macro vascular complications, including cardiovascular, peripheral vascular disease and cerebro vascular diseases.This investigation primarily concerns patients with T1DM.However, although T1DM and T2DM are usually considered quite separately, there are some similarities between the two conditions, both of these conditions will be considered in building this picture of antioxidant responses to oxidative stress in the pathogenesis of diabetes [2,3].Increasingly, T2DM is recognised as a proinflammatory state with an increased risk of macro and micro vascular disorders, due to oxidative stress.Increased oxidative stress is manifested by increased lipid peroxidation and in increased DNA damage [4,5], whereas T1DM manifests itself as an attack of autoreavtive T-cells against pancreatic beta cells but in many ways the two conditions overlap substantially with both resulting in the deterioration of glycaemic control [6].Patients with diabetes often suffer from cardiomyopathy, which cannot be explained by impaired cardio perfusion.Cardiovascular disease risk is two-to four-times greater in individuals with Type 2 Diabetes Mellitus (T2DM), relative to individuals without diabetes.Further, diabetes is accompanied by increased cellular inflammation, as evidenced by increased monocytic superoxide, cytokines and adhesion to endothelium [5].The essential beta cell dysfunction can be influenced by many factors, including hyperglycemia/glucotoxicity, lipotoxicity, autoimmunity, inflammation, adipokines, islet amyloid, incretins and insulin resistance that can all influence the function of pancreatic beta cells.The resulting hyperglycaemia induces an excessive production of reactive oxygen species (ROS) leading to chronic oxidative stress (OS) [7].Studies on islets isolated from pancreata of subjects with T2DM showed increased markers of AbstractDiabetes is a heterogeneous disease where many factors are involved in its pathogenesis.The genotype frequency of Catalase (CAT) microsatellite polymorphism in patients with Type 1-Diabetes (T1DM) was analysed.86 T1DM patients (37M: 49F) and 81 normal controls (43M: 38F) were included in the investigation.The diabetic controls (DC) had an average age of 34.0 years ± 2.84 SEM (n=7, 3M: 4F), a mean duration of disease of 27.9 years ± 2.46 SEM and did not have any diabetic complications for at least 20 years.Patients with diabetic nephropathy (n=16, 7M: 9F) were on average 47.3 years ± 5.54 SEM and had been diagnosed for 30.8 years ± 2.94 SEM.There was also a group of patients that had been diagnosed for a short duration (SD) with a mean age of 21.7 years ± 2.60 SEM (n=8, 5M: 3F).A further 55 patients (21M:24F) had been diagnosed for 18.4 years ±1.30SEM; mean age of 26.7 years ± 1.13SEM but no complications were recorded and not eligible to be included in the DC group being diagnosed for less than 20 years.Significant differences reported between patients with diabetes (n=86, 37M: 49F) and normal healthy controls (n=81,43M:38F).Patients with diabetes had a higher percentage of heterozygous copies (54%; Chi-square=5.87;p=0.01); normal controls had a higher homozygous percentage (63%; Chi-square=6.5;p=0.01). ConclusionThis is the first reported polymorphism of CAT that may be associated with the cellular damage causing the onset of diabetes

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